Different Regulation of Connexin26 and ZO-1 in Cochleas of Developing Rats and of Guinea Pigs with Endolymphatic Hydrops

Abstract

Using confocal microscopy and morphometry, we analyzed the expression of connexin26 (Cx26) and ZO-1 in rat cochlea during the postnatal period to elucidate spatiotemporal changes in gap junctions and tight junctions during auditory development. We also studied changes in these junctions in experimental endolymphatic hydrops in the guinea pig. In the adult rat cochlear lateral wall, Cx26 was detected in fibrocytes in the spiral ligament and in the basal cell layer of the stria vascularis, whereas ZO-1 was detected in the apical surfaces of marginal cells and in the basal cell layer. During postnatal development, Cx26 expression increased mainly in the spiral ligament, whereas ZO-1 expression increased in the basal cell layer. The morphometry of Cx26 showed a sigmoid time course with a rapid increase on postnatal day (PND) 14, whereas that of ZO-1 showed a marked increase on PND 7. In experimental endolymphatic hydrops, the expression of Cx26 significantly decreased, whereas there were no obvious changes in the expression of ZO-1. These results indicate that gap junctions and tight junctions in the cochlea increase in a different spatiotemporal manner during the development of auditory function and that gap junctions and tight junctions in the cochlea are differentially regulated in experimental endolymphatic hydrops. (J Histochem Cytochem 49:573-586, 2001)

Roles of gap junctions in glucose transport from glucose transporter 1-positive to -negative cells in the lateral wall of the rat cochlea

“…3b). These results are consistent with those of our previous studies (Suzuki et al 2001(Suzuki et al , 2003. In the stria vascularis, GLUT1 was closely associated with abundant Cx26-immunolabeled spots in the basal cell layer (Fig.…”

“…Gap junctions and tight junctions were detected in the cochlea by electron microscopy (Forge 1984;Jahnke 1975;Nadol et al 1976;Reale et al 1975;Spicer and Schulte 1996), and the immunolocalization of the gap junction proteins connexin26 (Cx26), connexin30 (Cx30), connexin31 (Cx31) and connexin43 (Cx43) has been reported (Kikuchi et al 1995;Lautermann et al 1998;Suzuki et al 2001Suzuki et al , 2003Xia et al 2000). The immunolocalization of the tight junction proteins such as claudins, occludin, and ZO-1 has also been reported (Florian et al 2003;Kitajiri et al 2004;Suzuki et al 2001).…”

“…The immunolocalization of the tight junction proteins such as claudins, occludin, and ZO-1 has also been reported (Florian et al 2003;Kitajiri et al 2004;Suzuki et al 2001). The crucial roles of gap junctions and tight junctions in auditory functions have been conWrmed by the discoveries that mutations of the Cx26 (Kelsell et al 1997), Cx30 (Grifa et al 1999), Cx31 (Liu et al 2000;Xia et al 1998), and claudin-14 (Wilcox et al 2001) genes are responsible for some cases of human hereditary sensorineural deafness.…”

Gastric type H+,K+-ATPase in the cochlear lateral wall is critically involved in formation of the endocochlear potential

“…7B) (31,65). IS is electrically isolated with two tight-junction shields: the marginal cell layer and the basal cell layer (19,33,39,40,78). Intermediate and basal cells are connected through gap junctions not only to each other but also to fibrocytes, endothelial cells, and pericytes (38,80).…”

A Case against Spiral Ligament Atrophy as a Cause of Ménière’s Disease

“…K in perilymph might also enter the spiral ligament and be shuttled through type IV fibrocytes and type I fibrocytes to enter the stria vascularis and then the endolymph [13]. Examination of Cx26 expression by immunohistochemistry in an experimental model [19] of endolymphatic hydrops showed a decrease in expression perhaps contributing to the hydrops by changing the relative K concentration in the two fluids [20]. The Na,K-ATPase, however, does not seem to be affected in Ménière's disease [21] or in experimental endolymphatic hydrops [22,18].…”